Tag Archives: cardiac arrest

Should we regionalize post-arrest care? Well, if your facility does not have a cath lab, then the answer is yes. But Academic Hospital A, which sees >100 arrests a year, just started advertising a fancy post-cardiac-arrest service. Academic Hospital B also sees >100 arrests a year, but does not have a post-arrest service aside from their MICU.

You, being at hospital C without a cath lab, have just achieved ROSC in a witnessed arrest. Who do you transfer to?

This study looks at 987 post-arrest patients that survived to admission at 7 hospitals in and around Southwestern Pennsylvania. One of them is a regional referral center with post cardiac arrest services consulted on OHCA with ROSC, accepts sudden cardiac arrests from outside facilities, and is consulted on in-hospital arrests with ROSC. There are two additional tertiary care centers that see >100 SCA annually, and 4 “low volume” centers. They look at multiple variables, and evaluate discharge disposition, discharge CPC, and length of survival post-discharge.

They improved numbers of discharge CPC – the post arrest service center with a discharge CPC of 1 or 2 32% of the time vs 37% of the time for the other 6 facilities. More patients were discharged to home (41% vs 32%) from the post-arrest service center and survived for longer if they were treated with the post-arrest service.

Now….

While the authors claim similar patient characteristics between the post-arrest service center and the other 6 hospitals…. 46% of patients were transferred to the post-arrest service center vs 16% at hospitals 2-7 – perhaps skimming a healthier patient that made it through the transfer (remember- you had to survive to discharge to be counted) – the authors even acknowledge that their transferred patients did better than their other arrests.

Add in that the initial rhythm 51% of the time was VT/VF for the post-arrest service center vs 41% in the other six hospitals, and you’ve got plenty of confounders. Frankly, given all of this, it’s a bit strange that the proportion of patients surviving to discharge did not differ at all. One would think if you have a post arrest service and the scales are tipped in your favor to begin with, that you’d have a higher percentage of patients surviving.

Ultimately, patients lived longer post-arrest when treated at a facility with a post-arrest service, and the authors are touting this as reason to (further) regionalize post-arrest care. Sure, there are slightly better neurologic outcomes, but the scales were tipped in their favor to begin with. I don’t trust this conclusion, especially when the post-arrest service had an advantageous patient population to begin with that should have led to a measurable increase in improved survival, in addition to an increase in length of survival.

This study demonstrates what many of us have probably suspected – the absence of cardiac activity on ultrasound portends a grave diagnosis; but this study really is so much more.

Utilizing 20 sites across the US and Canada from May 2011-Nov 2014 looked at all nontraumatic in-ED and out of hospital cardiac arrests that arrived to the ED in either PEA or asystole, and whether or not POCUS demonstrated a potential role in resuscitation.

953 patients, 793 used for final analysis (106 not included due to resuscitation under 5 minutes, 8 patients DNR, 1 uninterpretable sono, 3 with incomplete timing data, 42 for no ACLS meds given) – had a cardiac sono at the “beginning and end of ACLS.” The primary outcome was percentage of patients that survived to hospital admission, with secondary outcomes of survival to discharge and ROSC. Unfortunately, neurologic intact survival was not evaluated. The treating EP’s were credentialed in POCUS at their local institutions and unblinded. Digital clips were reviewed by a single reviewer in a blinded fashion for agreement (which was deemed to be “substantial agreement”).

The data (numbers are percentage, such that “28.9” = the percentage of patients with cardiac activity on POCUS during the resuscitation who survived to admission):

Cutting to the chase, this study brings up a number of key points:

-PEA on the monitor may not necessarily be PEA, with a whopping 54% of patients having cardiac activity on POCUS

-asystole on the monitor may not be cardiac standstill, as 10% had cardiac activity on POCUS

– cardiac activity on POCUS for PEA/asystole portends only a 3.8% survival to discharge

-no cardiac activity = poor prognosis, 0.6% of patients survived (3 out of 530). With two of the three patients were Vfib at some point during EMS working on them.

-pericardial effusion was seen in 34 patients (4.3% of those in the final analysis). 15.3% of patients whom had a pericardiocentesis performed survived to discharge.

– only 15 patients received lytics for suspected PE, with only one (6.7%) surviving to discharge. (which was almost the MORTALITY rate of PEAPETT)

Whew. This is a lot to digest. Let’s just say that ultrasound helps you tease out a spectrum of disease and further characterizes what you are dealing with. I’m looking at POCUS in codes as a risk stratification tool. Is there a prolonged time without cardiac activity without a potentially reversible causes? Might want to consider calling it earlier since survival to discharge is abysmally low. And sheesh… 1 out of 25 cardiac arrests had a pericardial effusion??? Wow. Time to brush up on those pericardiocentesis skills.

Caveats- this was done by EP’s credentialed for POCUS, so they’re likely more talented than the rest of us. Dont let that scare you though, rather, this. Perhaps seeing cardiac movement on ultrasound lends a “bridge to hope” and the team puts in a more-heroic-than-usual effort.

And of course, this also leads to more questions- of those 28.9% with cardiac activity that survive to admission, what if they are brought straight to the cath lab? Or started on ECMO? Would this potentially alter survival rates and neurologically intact survival in meaningful ways? Time shall tell. Until then, cut that KT window, pick up the probe, and have your TPA & long pericardiocentesis needle ready.

This paper puts those thoughts under the microscope a bit, and challenges us to think ahead and be prepared.

They looked at all OHCA from 2006 to 2012 with initial brady/asystolic arrests to determine if they may benefit from pre-hospital pacing, and to look at survival rates associated with various rhythms. Clear non-cardiac causes (trauma, drowning, respiratory, neurologic, suicide) were excluded.

7925 OHCA in the Netherlands

less non-cardiac (6681 patients)

less those without EKGs (~500 patients)

less ~3000 patients with VF/VT (now at 2643 patients)

less those with normo/tachycardia and those with pacers previously placed (~300 patients)

Unwitnessed arrest still protends a poor outcome, with survival about 0.5%. However, for witnessed arrests, they report 4% survival for idioventricular / junctional arrests and 6.8% for sinus brady arrests. This seems consistent with prior studies. However, for a study trying to determine whether or not pacing is beneficial, their pace rates were quite low. They paced 11 of 220 sinus brady patients and 41 of 452 idioventricular / junctional patients, with a delay of 30.1 and 16.5 minutes to pacing respectively – with an electrical capture rate of 55% and 70% to boot. Esssentially, they can’t answer the question “Does pacing help” with such a care gap.

So, why is this? For sinus brady, maybe patients are hanging in the 40’s-50’s and felt to be quasi-stable. Maybe its the angst of floating a pacer. Perhaps the lengthy delay for sinus brady is giving atropine, then giving it again… and maybe again- akin to pressor-angst for sepsis (giving a 4th, 5th, and 6th liter rather than starting pressors or a central line). I imagine there is a mental barrier – whether it be not thinking about pacing or passing the buck (“I’ll let the ICU figure it out.”). The evolution of the ED-ICU model (and perhaps UPMC’s cardiac arrest unit) may be the best place to look at this type of “full bore” medicine and whether or not it would be beneficial.

But for now, there is a large gap in care. Bradycardic arrests represent about 10% of arrests, have a reasonable survival rate, and are (potentially) suboptimally managed – and you have the tools to potentially improve an outcome. We can not say whether or not pacing is futile care for this condition.

Until then, go full bore. Your patients & their families deserve it until pacing is demonstrably shown to not be beneficial in bradycardic arrests.

So a few weeks ago, I asked the Twittersphere whether or not ultrasound should be readily available (if not outright used) in all codes. The answer was a resounding yes, and today’s article helps support that claim.

49 ICU patients with cardiopulmonary arrest (asystole or PEA) underwent intra-arrest bedside TTE. Based on Echo findings, these patients were classified as either asystole, PEA without cardiac contractility, or PEA with cardiac contractility. ROSC and survival to discharge, and survival to 180 days were evaluated. Of these 49 patients, 17 (35%) were in asystole based on Echo, 5 (10%) were in PEA without cardiac contractility, and 27 (55%) were in PEA with cardiac contractility. Rates of ROSC were 23.5% for those in asystole, 20% for PEA without cardiac contractility, and 70.4% for those in PEA with cardiac contractility. Survival to discharge (22%) and after 180 days (15%) only occurred in the PEA group with cardiac contractility. (Full disclosure- no word on CPC neurologic outcomes for survivors).

Now, this study looks at ICU arrests – clearly a bit different from OHCA cases we see in the ED, and perhaps intrigues me to suggest using cardiac POCUS in OHCA to stratify the futility of the resuscitation (This review found significant bias and large heterogeneity for prehospital sono usage for arrests). Nevertheless, with 15% 6-month survival in a group that without bedside sono you would call the code – its time to seriously consider the use of ultrasound (at least for) cardiac evaluation in all codes. For all of the things we do that fall into the “can’t hurt, might help” category, ultrasound in an arrest has to be high on the list.

Welcome to the Twelve Trials of Christmas series on EMinFocus! This is the tenth of twelve posts in a series where I ramble on various topics for which I would love to see an EM study done. I’ve taken morsels of prior studies (case series, small trials, etc) and highlight reasons on why I believe this study would benefit EM. Some may pan out, some may not. All of them I would be highly interested in assisting with in any way possible to continue to advance our fine specialty.

Even after a successful initial resuscitation of a cardiopulmonary arrest, there is then significant concern for the patients neurological outcome. Sure, there is the hypothermia protocol, but is there any other neuroprotective drugs that we may be able to trial post arrest to try and improve neuro outcomes?

Let’s first say this: we’re talking about mouse studies, so it’s a leap of faith. However, levetiracetam is quite safe, and really, what harm, post arrest, could a few doses of Keppra for the first 72 hours really do? In mouse models, its been shown to have neuroprotective effects in experimental stroke, ICH, and neurotrauma. ( 1 , 2 )

There was a study published in March 2014 in regards to anti-epileptics (phenytoin, levetiracetam, valproate, clonazepam, propofol, midazolam), which showed no measurable difference when administered to patients post-arrest. However, in this study, patients were already placed in the ICU and the requirement was to be placed on continuous EEG monitoring within 12 hours of hospital presentation. If the EEG was positive, they were enrolled in the study, and initiated on some anti-epileptic (being on propofol post intubation, apparently allowed them into the protocol under the propofol group). Essentially, this study is useless to the ED and should not stray us from doing a good study to begin Levetiracetam as early as possible in cardiac arrests. We know that the later we attempt to reverse status epilepticus, the more difficult a time we will have(and here, they didn’t attempt for HOURS!), so why not make a good attempt at giving arrests the best possible outcome with an easy study? Hang a bag of Levetiracetam vs a bag of saline on all arrests, those that survive, compare neurologic outcomes. This is an easy one to pass through the IRB – cant hurt, may do a world of help.

Its 2034, yet your ED is still receiving EMS calls via telephone to the charge nurse. EMS is 4 minutes out with a witnessed arrest of a 54 year old male downtown that occurred 8 minutes ago. The patients wife was able to quickly state that the patient had no known medical problems, and that the patient had said he “felt funny,” grabbed his chest, then arrested. EMS found him to be pulseless and in ventricular fibrillation. ACLS is initiated in the field & continued en route, and the charge nurse activates the mobile ECMO lab.

In February 2014 Resuscitation, Sakamoto et al. treated out of hospital cardiac arrest patients with VF/VT on the initial EKG with a treatment bundle including ECMO-CPR, hypothermia, and intra-aortic balloon pump vs conventional CPR. The results?

I’ll admit, I’m not terribly familiar with ECMO, other than what I’ve seen on twitter, on EDECMO.org, and on YouTube. By the end of my career, I could see the above scenario being common at tertiary centers – much like pre-hospital cath lab & stroke team are activated now.

We should care about end tidal CO2 during CPR as it can depict the respiratory process (ie, metabolism, transport, ventilation) even in a low perfusion state. As such, there are 3 good reasons (if not more!) to monitor ETCO2 during an arrest.

Monitoring CPR Fatigue

During effective CPR, ETCO2 values are typically 10-20 mmHg. A trend down may indicate fatigue of the person providing chest compressions. I think we’ve all seen when the person providing CPR is sweating and too shy to say they need a rest. Give ’em a break.

<10 for 20? Call it.

Values persistently at 10 mmHg or under for 20 minutes of CPR are 88% sensitive and 77% specific for not obtaining ROSC. The grey area – those between 10 & 20 mmHg, is less clear. There is conflicting literature that 14-15 mmHg should be a stopping point. One study of 737 patients found, “When a 20-minute end-tidal carbon dioxide value of 1.9 kPa (14.3 mmHg) or less was used as a screening test to predict ROSC, the sensitivity, specificity, positive predictive value, and negative predictive value were all 100%” where as another found: “We identified 22 patients, who had an initial end-tidal CO2 at or below 1.3kPa [9.75 mmHg]. Four of these patients achieved return of spontaneous circulation.” No comments on whether or not these 4 patients survived to discharge. Good review found here: http://www.ncbi.nlm.nih.gov/pubmed/23871864

Predicting ROSC

When you see sudden bump- typically 10mmHg or >35mmHg- Congrats! – you’ve got ROSC. Now, no one needs to have their hand in the patients groin to do frequent pulse checks. And no one needs to stop CPR. CAUTION: this is a single study of 108 patients and stands to be the foundation of new dogma.

Final thought, and one that may actually make a difference…

values in mean ± SD (from Resusc 2012 paper below)

The standard deviation numbers have significant overlap. However, a lower ETCO2 after ROSC brings forth the question of thrombolysis for PE. And would you have thrombolysed anyway after a RUSH exam and an EKG showing right sided strain?

The gist: ETCO2 is now in the ACLS guidelines and on the EMS wagons, time to get our EDs up to speed